Our group has recently demonstrated that the HDACi vorinostat, in combination with the EGFR-tyrosine kinase inhibitor gefitinib, induced synergistic inhibition of proliferation, migration and invasion as well as induction of apoptosis, in preclinical models of SCCHN and NSCLC, including cancer cell lines resistant to gefitinib and characterized by mesenchymal markers and phenotype. The gene discussed is EGFR; the disease is head and neck squamous cell carcinoma.